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MDENT110 > Blood > Flashcards

Blood Flashcards

1
Q

How much of the blood is plasma?

A

55%

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2
Q

How much of the blood is RBC?

A

45%

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3
Q

How much of the blood is the buffy coat?

A

less than 1%

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4
Q

What is the buffy coat made up of?

A

leukocytes and platelets

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5
Q

What do macrophages differentiate from?

A

Monocytes

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6
Q

What do basophils, eosinophils, neutrophils and monocytes differentiate from?

A

Myeloblasts

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7
Q

Where does haematpoeisis occur?

A

Bone marrow

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8
Q

Where does haematopoeisis occur in an embryo?

A

Yolk sac then liver and spleen

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9
Q

What is the lifespan of RBC?

A

120 days

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10
Q

What is the life span of white blood cells?

A

6 hours

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11
Q

What is the lifespan of platelets?

A

7-10 days

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12
Q

What are old/dying cells removed by?

A

Spleen

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13
Q

What stimulates and controls blood cell production?

A

Hormones

Red cells: erythropoietin (EPO)
White cells: granulocyte colony stimulating factor (GCSF)
Platelets: thrombopoietin (TPO)

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14
Q

What is erythropoietin?

A

a hormone produced by the kidney that promotes the formation of red blood cells by the bone marrow. The kidney cells that make erythropoietin are sensitive to low oxygen levels in the blood that travels through the kidney

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15
Q

What shape is RBC?

A

biconcave disc

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16
Q

What does haemoglobin carry?

A

Oxygen

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17
Q

How many RBC in blood?

A

4x10^12/L

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18
Q

What is a polycythaemia?

A

Increase in red cells:
Raised erythropoietin
Hypoxia

Reduction in plasma volume:
Dehydration
Smokers

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19
Q

What are platelets made from?

A

Megakaryocytes in bone marrow

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20
Q

What is the normal platelet range?

A

140-400x10^9/L

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21
Q

What is the condition called for low platelets?

A

thrombocytopenia

Platelets <80 increased risk of bleeding
Platelets < 20 spontaneous bleeding / bruising

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22
Q

What is the condition called for high platelets?

A

thrombocytosis

Increased rates of arterial and venous thrombosis

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23
Q

What do neutrophils do?

A

Phagocytose and kill bacteria

Increased in bacterial infections (neutrophilia)

Release cytokines which cause inflammatory response eg temperature

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24
Q

What do coagulation factors convert?

A

Convert soluble fibrinogen into insoluble fibrin polymer

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25
Q

What are the 2 most important systems of red cell antigens?

A

ABO and Rhesus

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26
Q

What are the Rhesus blood groups?

A

Complex system of C, D and E antigens

D is the most important

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27
Q

Why is anti-D important?

A

pregnant women given anti D to prevent sensitisation. The anti-D immunoglobulin neutralises any RhD positive antigens that may have entered the mother’s blood during pregnancy. If the antigens have been neutralised, the mother’s blood won’t produce antibodies.

Rhesus disease can largely be prevented by having an injection of a medication called anti-D immunoglobulin. This can help to avoid a process known as sensitisation, which is when a woman with RhD negative blood is exposed to RhD positive blood and develops an immune response to it.

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28
Q

What are the indications of blood transfusion?

A

Hypovolaemia due to blood loss

Severe anaemia with symptoms due to inadequate tissue oxygenation (transfusion trigger often = 80 g/L)

Anaemia that cannot be corrected by bone marrow function

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29
Q

When is blood transfusion not indicated?

A

Not indicated for iron deficiency or B12/ folate deficiency.
Not indicated for minor blood loss, especially if fit and healthy
Not indicated for asymptomatic anaemia

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30
Q

What are the risks of a blood transfusion?

A

ABO incompatibility reaction – can be rapidly fatal
Delayed transfusion reactions
Fever, hives
Fluid overload, pulmonary oedema

Infections:
Bacterial
Viral (HIV, hepatitis B and C)
Malaria
Prions (vCJD)

Long term – iron overload: damage to heart, liver

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31
Q

What cells does HIV invade?

A

CD4 cells

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32
Q

What is leukaemia?

A

Malignancy of (white) blood cells

Acute leukaemia: proliferation of immature cells without differentiation

Chronic leukaemias: proliferation with differentiation

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33
Q

What are the symptoms of leukaemia?

A

Anaemia (fatigue, pallor)
Neutropenia (infections)
Thrombocytopenia (bleeding & bruising)

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34
Q

Which cells does acute myeloid leukaemia affect?

A

Myeloblast

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35
Q

Which cells does acute lymophoblastic leukaemia affect?

A

Common lymphoid progenitor

36
Q

Which cells do chronic myeloid leukaemia affect?

A 
Megakaryocyte
basophil
neutrophil
eosinophil
monocyte
37
Q

Which leukaemia primarily affects children?

A

Acute lymphoblastic leukaemia - chemo 2-3 years

38
Q

What is the treatment for acute myeloid leukaemia?

A

High dose chemo, possible bone marrow transplant

39
Q

What causes chronic myeloid leukaemia?

A

Translocation between chromosomes 9 and 22

Forms “Philadelphia” chromosome

40
Q

What is the treatment for chronic myeloid leukaemia?

A

Targeted therapy (tablets)
Imatinib
Survival – similar to general population

41
Q

What is the treatment for chronic lymphocytic leukaemia?

A

Gentle, outpatient chemotherapy
More targeted oral treatments becoming available
Survival – several decades

42
Q

What causes chronic lymphocytic leukaemia?

A

Proliferation of mature lymphocytes (usually B cells)

43
Q

What is lymphocytosis?

A

a high lymphocyte count, is an increase in white blood cells called lymphocytes.

44
Q

What is lymphoma?

A

Malignancy of lymphoid cells, predominantly in lymph nodes

45
Q

What are the two types of lymphomas?

A

Hodgkin’s lymphoma

Non Hodgkin lymphoma

46
Q

How is high grade lymphoma treated?

A

Aggressive, acute, treat with chemotherapy / curable

47
Q

How is low grade lymphoma treated?

A

Chronic, indolent, may not require treatment / incurable

48
Q

What is a Myeloma?

A

Malignant proliferation of plasma cells

Produces monoclonal immunoglobulin (paraprotein)

49
Q

What are the clinical features of myeloma?

A

Calcium (hypercalcaemia – bone pain, constipation)

Renal failure

Anaemia

Bone lesions (lytic lesions, fractures, pain)

50
Q

What is the treatment for myeloma?

A

Treatment – outpatient, mainly oral chemotherapy

51
Q

What are the two methods of creating an intravascular solid?

A

Coagulation - protein level

Platelets - cellular level

52
Q

What are the 2 pathways of coagulation?

A

Intrinsic pathway

Extrinsic pathway

coalesce to form same final common pathway

53
Q

What is the intrinsic pathway triggered by?

A

Negatively charged molecules from endothelial trauma (phospholipids released into blood) and factor XII (9) - this activates coagulation on the inside of the vessel

54
Q

What is the extrinsic pathway triggered by?

A

Blood starts leaking out - comes into contact with subendothelial tissue just under endothelial layer, which contains collagen that activates the extrinsic pathway

55
Q

What reaction happens at the end of the coagulation cascade

A

FIbrongen –> fibrin by an enzyme

56
Q

Which test measures the extrinsic pathway and the final common pathway?

A

Prothrombin time -PT

INR - international normalised time

57
Q

Which test measures the intrinsic pathway and the final common pathway?

A

APTT - activated partial thromboplastin time

58
Q

How is blood stopped from coagulating when taking it to measure it? and how is this reversed in the lab?

A

Blood collected in CITRATE - lemon juice

this chelates Ca2+ (removes)

Ca2+ is clotting factor IV; required for both intrinsic and extrinsic pathways

In lab, an excess of Ca2+ is added to overcome citrate and then other things are added to activate either extrinsic or intrinsic pathway
tissue factor for extrinsic
phospholipid for intrinsic

59
Q

How is prothombin time measured?

A

Tissue factor added to blood sample in lab, and time how long to clot

Measure factors I, II, VII and X (1, 2, 7, 10) - 2, 7, 9, 10 - inhibited by warfarin

60
Q

What is INR?

A

Patient’s PT: normal PT

Under specific laboratory conditions - 25 degree c at sea level etc
Used to assess Warfarin’s effect

INR of 2 - patient’s extrinsic pathway of coagulation is twice as long under specific laboratory condition

61
Q

What is APTT?

A

Activated Partial Thromboplastin Time
Phospholipid, silica & Ca2+ added to sample

Time how long to clot formation
- measure intrinsic and final common pathway

  • measures factors I, II, V, VIII, IX, X, XI, XII
    2, 9, 10 - warfarin also affects APTT but not measured
    VIII (8) and IX deficiency (9) - haemophilia
62
Q

Which factors that are deficient cause haemophilia?

A

VIII (8) and IX deficiency (9) - haemophilia - prolonged APTT, normal PT

63
Q

What are the causes of haemostatic problems?

A

Congenital bleeding disorders:
- Haemophilia - A = factor 8 deficiency VII
B - factor 9 deficiency IX
(increased APTT)

  • von willebrand’s - shortage of VWBF which are important in platelet adhesion - which increases bleeding time (marker of platelet function), VWBF binds to factor 8 and stops it being broken down in the blood which causes increased APTT

Acquired bleeding disorders:
- medical conditions:
Liver:
- cancer. cirrhosis/jaundice, paracetamol overdose (PT is the first marker of the failing liver)

Kidney:

  • related to platelet function not number
  • prolonged bleeding time
  • will be on heparin (blood thinner) during dialysis, if they need a tooth out, schedule for non-heparin day.

Cardiac (due to drugs…)

Cancer (due to drugs or myelosupression - bone marrow suppressed, RBC and platelets production lower)

ITP - immunothromboperpura, ITTP - idiopathic version of the above

  • drugs:
  • warfarin
    -aspirin
    -clopidogrel
    -heparin
    new, more predictable so don’t need regular weekly INR tests:
  • dabigatran (direct thrombin inhibitor)
  • rivaroxaban (directed activated factor X)
64
Q

Where are all vitamin K dependent coagulation factors produced?

A

In the liver

liver makes most coagulation factors - all vitamin K but other non vitamin K factors produced here too

65
Q

Where is aspirin first metabolised?

A

Liver - main therapeutic effect needs to be within hepatic portal vein before reaching liver because liver will take it out

66
Q

What is the reason for efficacy of aspirin?

A

Reason for efficacy is IRREVERSIBLE INACTIVATION of COX within platelets - platelet function is reduced

Lasts the life of the platelet

Reversal requires 7 days of discontinuation

67
Q

What is the simplified Arachidonic acid pathway?

A

arachidonic acid is metabolised into other things in inflammation e.g. leukotrienes - attracts wbc

metabolisd into prostaglandins via COX 1, 2, 3- pain and regulated gastric regulation

metabolised into thromboxane A2, TXA2 - platelet aggregating factor attracts other platelets, if blocked irreversibly, then antiplatelet effect

68
Q

What does vitamin K do to factors 2, 7, 9, 10 and Protein C and S?

A

Activates them when vitamin K changes to vitamin K epoxide

vitamin K is co-factor for this reaction

then vitamin K epoxide turns back to vitamin K via vit K epoxide reductase

warfarin blocks vit K epoxide turning back so factors aren’t becoming active - coagulated state

A lot of vitamin K can reverse effects of warfarin to drive reaction forward and produce more active factors

69
Q

What does heparin bind to?

A

Binds to and activates antithrombin III - this molecules blocks factor 10 and 2

70
Q

What chemical reverses heparin?

A

protamine sulphate

71
Q

How does clopidogrel work?

A

Affects platelet function

it’s a P2Y 12 inhibitor - important receptor of the platelet

P2Y12 involved in platelet aggregation and linking to the fibrin meshwork

72
Q

How can you avoid haemorrhage in certain patients?

A

Warfarinised patient

  • check INR within 72hrs of procedure
  • INR <4 (if greater than 4, don’t take tooth out)
  • avoid ID blocks where possible

Antiplatelets patient (aspirin, clopidogrel, dipyridamole)

  • monotherapy - continue as planned
  • if on multiple drugs, no evidence of increases bleeding risk but may consider hospital-based treatment

Haemophilia/VWB

  • Liase with haematologist
  • give DDAVP - for haemophilia A desmopressin
  • Recombinant factor A - VIII/ B - IX
  • mild may need no preoperative management
  • Tranexamic acid - procoagulant afterwards

NOACS: SDCEP guidelines - exam question

  • if 3 more more teeth, or if surgical extraction carry on as normal
  • once a day med - stop on morning of surgery, then take 4 hour after extraction
  • twice a day med - generally omit morning dose
73
Q

What are the types of haemorrhage

A

Primary
– as soon as tooth is removed
– will be due to bleeding disorder or local cause

Reactionary
– not immediate, but within 48hrs of extraction
– ETOH, exercise, heat, anaesthetic wearing off

Secondary
- approximately 1 week after surgery, due to infection e.g. ENT

74
Q

What are the standard measures to achieve haemostasis in any tooth?

A
  • firm pressure/ bite on gauze
  • compress socket
  • post-op instructions (reactionary haemorrhage)
75
Q

What are the 2 potential sources of bleeding after an extraction?

A
  1. Bone - haemostatic pack in socket
  2. Gingivae- suture

Do both

76
Q

What can you use to pack the bone?

A

Surgicel
- resorbable oxidised cellulose
helps clot form

Gelatin sponge
- absorbs up to 45 times own weight in blood
pressure tamponades bleed

77
Q

How does suturing help achieve haemostasis?

A

Will compress gingival blood supply, stemming soft tissue bleed

Also will act to prevent haemostatic pack from falling out

78
Q

How can you manage an ongoing bleed? (drugs)

A

Tranexamc acid

May need reversal of anticoagulant if possible

  • warfarin - omit/vitamin K given
  • Heparing - omit/protamine sulphate given

Need to weigh up against risks of thrombosis, and is actually very rarely done where INR has been correctly checked pre-op

Accept very small amount of oozing for a few days if known bleeding disorder

79
Q

What tests would you do if there was an ongoing bleed of an unknown cause?

A
  • Coagulation screen/ bleeding time
  • Full blood count (platelets)
  • Factor assay
80
Q

How does aspirin have its effects?

A

Irreversible inhibits COX, preventing TXA2 formation and therefore platelet aggregation

81
Q

What blood test is INR a ratio of?

A

PT - prothrombin time

82
Q

Give 4 measure to deal with haemorrhage from a dental socket

A 
Pressure/bite on gauze
stitch
pack
Tranexamic acid
Local anaesthetic injection - vasoconstriction adrenaline
83
Q

How is the action of warfarin reversed in a severe, life threatening event?

A

Vitamin K, 2-10mg

84
Q

How does DDAVP react?

A

Induces release of factor VIII from a vascular endothelia into circulation

85
Q

What other names are there for DDAVP?

A

Desmopressin
Synthetic vasopressin
Synthetic ADH

MDENT110 (26 decks)

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